HP1021 is a redox switch protein identified in Helicobacter pylori

Author:

Szczepanowski Piotr1,Noszka Mateusz1ORCID,Żyła-Uklejewicz Dorota1,Pikuła Fabian1ORCID,Nowaczyk-Cieszewska Malgorzata1ORCID,Krężel Artur2ORCID,Stingl Kerstin3,Zawilak-Pawlik Anna1ORCID

Affiliation:

1. Department of Microbiology, Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wrocław 53-114, Poland

2. Department of Chemical Biology, Faculty of Biotechnology, University of Wrocław, Wrocław 50-383, Poland

3. Department of Biological Safety, National Reference Laboratory for Campylobacter, German Federal Institute for Risk Assessment, Berlin 12277, Germany

Abstract

Abstract Helicobacter pylori is a gram-negative, microaerophilic, pathogenic bacterium and a widespread colonizer of humans. H. pylori has developed mechanisms that enable it to overcome the harsh environment of the human stomach, including reactive oxygen species (ROS). Interestingly, up to now no typical regulator dedicated to the oxidative-stress response has been discovered. In this work, we reveal that the inhibitor of replication initiation HP1021 functions as a redox switch protein in H. pylori and plays an important role in response to oxidative stress of the gastric pathogen. Each of the two predicted HP1021 domains contains three cysteine residues. We show that the cysteine residues of HP1021 are sensitive to oxidation both in vitro and in vivo, and we demonstrate that HP1021 DNA-binding activity to oriC depends on the redox state of the protein. Moreover, Zn2+ modulates HP1021 affinity towards oriC template DNA. Transcription analysis of selected H. pylori genes by RT-qPCR indicated that HP1021 is directly involved in the oxygen-dependent control of H. pylori fecA3 and gluP genes, which are implicated in response to oxidative stress. In conclusion, HP1021 is a redox switch protein and could be a target for H. pylori control strategies.

Funder

National Science Centre, Poland

Hirszfeld Institute of Immunology and Experimental Therapy

Publisher

Oxford University Press (OUP)

Subject

Genetics

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